血清白细胞介素-6、白细胞介素-17和基质金属蛋白酶9水平与一氧化碳中毒迟发性脑病的关系  被引量:6

The relationship between the level of interleukin-6, interleukin-17 matrix metallo proteinase 9 and delayed encephalopathy after acute carbon monoxide poisoning

在线阅读下载全文

作  者:陈艳荣[1] 李晓[1] 徐化利 潘双双[1] 李丽[1] 

机构地区:[1]滨州市中心医院神经内科,251700,

出  处:《国际免疫学杂志》2016年第1期44-46,共3页International Journal of Immunology

摘  要:目的 探讨白细胞介素(IL)-6)、IL-17和基质金属蛋白酶9(MMP9)与一氧化碳中毒迟发性脑病(DEACMP)的关系.方法 随机抽取58例体检健康人群为对照组,抽取71例DEACMP患者为实验组,采用酶联免疫吸附试验(ELISA)检测DEACMP患者血清中IL-6、IL-17和MMP9的表达水平.结果 和对照组相比,轻重度DEACMP患者血清中IL-6和MMP9表达水平升高(F=22.47、F=36.51,P<0.05),其中在重度DEACMP患者血清中升高最显著;IL-17表达水平未有显著变化,差异无统计学意义(F=19.62,P>0.05).Pearson相关分析显示,DEACMP患者血清IL-6和MMP9浓度呈正相关(r=0.58,P<0.05).结论 DEACMP患者血清中IL-6和MMP9的表达水平与一氧化碳中毒的程度和预后密切相关.Objective To explore the relationship between the level of IL-6,IL-17 and matrix metallo proteinase 9 (MMP9) with deleyed encephelopathy after aucte carbon monoxide poisoning metal protease (DEACMP).Methods Rarcdomly selected 58 healthy people and 71 (delayed encephalopathy after acute carbon monoxide poisoning,DEACMP) patients were taken as control and experimental group,respectively.Enzyme-linked immunosorbent assay(ELISA) was used to detect the expression of IL-6,IL-17 and MMP9.Results Compared with control,the expression of IL-6 and MMP9 were significantly increased in mild and severe DEACMP patients,while both IL-6 and MMP9 showed largest increase in severe DEACMP patients with statistical significanc (F =22.47,F =36.51,P 〈 0.05).There was no significant expression changes of IL-17 (F =19.62,P 〉 0.05).Pearson analysis showed that the expressions of IL-6 and MMP9 were positively correlated with DEACMP (r =0.58,P 〈 0.05).Conclusions The expression of IL-6 and MMP9 in serum of DEACMP patients were associated with the degree of carbon monoxide poisoning.

关 键 词:一氧化碳中毒 迟发性脑病 白细胞介素 金属蛋白酶 

分 类 号:R595.1[医药卫生—内科学] R747.9[医药卫生—临床医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象